Małgorzata Rumińska

Cardiovascular diseases remain the leading cause of mortality worldwide, with multiple risk factors contributing to their development. Among these, obesity and hyperhomocysteinemia have been recognized as significant contributors to endothelial dysfunction, a key early event in the pathogenesis of atherosclerosis. Our study aimed to evaluate the relationship between total homocysteine (tHcy) levels and traditional cardiovascular risk factors in overweight and obese adolescents. We enrolled 42 obese, 14 overweight, and 25 non-obese children. No significant differences in tHcy levels were observed between overweight, obese, and non-obese adolescents. Homocysteine positively correlated with age (r = 0.433, p < 0.011) and creatinine concentrations (r = 0.363, p = 0.001) in the overall group of overweight, obese, and non-obese children, as well as in the combined group of overweight and obese children (for age: r = 0.275, p = 0.025; for creatinine: r = 0.278, p = 0.025). We did not find any association between homocysteine and atherogenic lipid profile, insulin-resistance status, blood pressure, and inflammatory parameters in overweight and obese patients. Age emerged as the strongest independent predictor of homocysteine levels. The observed association with creatine suggests a potential renal contribution to homocysteine metabolism.

Introduction: Childhood obesity contributes to the development of cardiovascular diseases. The molecular pathway – receptor activator of nuclear factor-κβ ligand (RANKL), its receptor RANK and osteoprotegerin (OPG) - takes part not only in bone metabolism but is also involved in the atherosclerosis process. RANKL stimulates osteogenic differentiation and calcification of vascular smooth cells. The associations between the OPG-sRANKL system and various cardiovascular risk factors were displayed. We aimed to evaluate the relationships between serum sRANKL (soluble RANKL) levels and the OPG/sRANKL ratio with cardiometabolic risk factors in overweight and obese children.Material and methods: The study included 70 children with overweight and obesity (mean age 13.0 ± 2.8) and 35 age-matched normal weight, healthy peers as a control group. In all patients, anthropometric measurements and laboratory tests were performed. Additionally, an oral glucose tolerance test (OGTT) was made only in overweight and obese children. Atherogenic and insulin resistance indices were calculated.Results: Overweight and obese children had lower sRANKL levels compared to the control group (median 276.95 vs 325.90, p=0.011), and consequently a higher OPG/sRANKL ratio (0.02 vs 0.01, p = 0.013). The studied children in the lowest quartile of sRANKL levels had higher body weight, Body Mass Index, waist circumference and increased glucose and insulin levels 60 minutes after OGTT and higher uric acid values compared to children in the highest quartile. In multivariable linear regression analysis sRANKL negatively correlated only with uric acid (β = - 0.508, p = 0.041). No association was found for the OPG/sRANKL ratio.Conclusion: Excess fat mass seems to alter the OPG/RANKL ratio mainly by reducing serum sRANKL levels. The correlation between sRANKL and uric acid may suggest a contribution of the OPG-sRANKL system in the cardiometabolic process, but that observation should be confirmed in future studies.

The alterations in thyroid function during recombinant human growth hormone (rhGH) treatment have been reported by many authors since this therapy became widely available for patients with growth hormone deficiency (GHD). Decrease of thyroxine level is the most frequent observation in patients treated with rhGH. This paper presents literature data describing changes in thyroid function related to rhGH therapy and a current explanation of mechanisms involved in this phenomenon. The effect of GH on the hypothalamic-pituitary-thyroid (HPT) axis is dependent on a multilevel regulation beginning from influence on the central axis, thyroid, and extra-thyroidal deiodinases activity as well as the impact on thyroid hormone receptors on the end. Changes in central and peripheral regulation could overlap during rhGH therapy, resulting in central hypothyroidism or an isolated slight deficiency of thyroxine. The regular monitoring of thyroid function is recommended in patients treated with rhGH and the decision of levothyroxine (L-thyroxine) supplementation should be made in the clinical context, taking into account thyroid hormone levels, as well as the chance for satisfactory growth improvement.

Background: Hypothyroidism in children leads to growth retardation. However, there is some evidence that recombinant human growth hormone (rhGH) therapy could suppress thyroid function. The most common observation in rhGH-treated patients is a decrease in thyroxine levels, which is reported as transient, but the studies in the field are inconsistent. We aimed to evaluate thyroid function in initially euthyroid children with idiopathic isolated GH deficiency during long-term rhGH therapy and to determine who is at a higher risk of thyroid function alterations during the therapy. Methods: The study group consisted of 101 children treated with rhGH for at least three years. Serum TSH and fT4 levels were determined at baseline, after the first six months and after each full year of therapy. The associations between changes in thyroid hormone levels during rhGH therapy and GH deficit, insulin-like growth factor-1 levels and growth response were investigated. Results: A significant decrease in fT4 levels (p = 0.01) was found as early as after the first six months of rhGH therapy. This effect persisted in the subsequent years of treatment without any significant changes in TSH values and tended to be rhGH dose related. Children with a greater fT4 decrease after the initiation of rhGH therapy were older, had higher bone age and responded to that therapy worse than children with lower fT4 changes. Conclusions: Our study revealed a long-term decrease in fT4 levels during rhGH therapy in initially euthyroid GHD children. The decrease in fT4 levels was associated with a lower growth response to rhGH therapy.

Introduction Osteoprotegerin has been shown to play a role in vascular calcification, atherosclerosis and the pathogenesis of cardiovascular diseases. We aimed to evaluate whether excess fat mass affects serum osteoprotegerin concentrations and to evaluate its associations with chosen cardiometabolic risk factors in overweight and obese children. Material and methods We enrolled 105 children ranging from 7.0 to 17.8 years of age. Among them 70 individuals were overweight and obese, and 35 were healthy with normal physical parameters. In all patients, anthropometric measurements and laboratory tests were performed. Atherogenic and insulin resistance indices were calculated. Results We did not find any differences in serum osteoprotegerin concentrations between overweight and obese children and their lean peers. In all studied patients, together with elevated quartiles of osteoprotegerin concentration, insulin resistance status decreased, and low-density lipoprotein cholesterol concentration increased. In the group of overweight and obese children osteoprotegerin was associated with low-density lipoprotein cholesterol, total cholesterol, and non high-density lipoprotein cholesterol. In the multiple linear regression analysis osteoprotegerin correlated only with low-density lipoprotein cholesterol (β = 0.140, p = 0.005). Conclusions Insulin resistance and lipid profile seem to influence circulating osteoprotegerin levels, but most likely needs more time to change its concentration in overweight and obese patients. The association of osteoprotegerin with low-density lipoprotein cholesterol may suggest its link with atherogenesis.

Introduction Obesity is a major health problem in Poland and around the world. Excessive gain in early childhood is an important risk factor for the development of obesity. The aim of the study was to analyze the prevalence of obesity in 2-, 4- and 6-year-old obese children. Material and...

Introduction: In the majority of countries, autoimmune thyroiditis is the main cause of acquired hypothyroidism in children. Typically, the natural course of the disease is initially insidious and the diagnosis is incidental. There are some children who develop severe hypothyroidism without a proper diagnosis. The aim of the study was to analyze the clinical and biochemical profiles of children with severe primary hypothyroidism due to autoimmune thyroiditis. Materials and Methods: We analyzed the records of 354 patients diagnosed between 2009 and 2019 with autoimmune thyroiditis. Only patients with TSH above 100 μIU/mL, associated with decreased free thyroxine and the presence of antithyroid antibodies, were enrolled in the study. The analysis encompassed clinical symptoms, thyroid and biochemical status, bone age, and imaging. Results: Twenty-six children were enrolled in the study. The mean age at diagnosis was 10.26 ± 3.3 years, with a female preponderance of 1.8:1. The most frequent symptom was growth impairment (77%) and weight gain (58%). Goiters were present in 42% of patients. Less common findings were pituitary hypertrophy (four patients) and hypertrichosis (three patients). Median values at the time of diagnosis were TSH 454.3 uIU/ml (295.0–879.4), anti-TPO antibodies 1,090 IU/ml, and anti-Tg antibodies 195 IU/ml. Anti-TSHR ab were evaluated only in six out of the 26 patients. The characteristic biochemical profile was correlated with the grade of hypothyroidism, and the strongest correlations were found with CBC parameters, lipid profile, aminotransferases, and creatine. Conclusion: In children with severe hypothyroidism, the most sensitive symptoms are growth arrest and weight gain despite the fact that, in some children, the auxological parameters at presentation could be within normal values for the population. The specific biochemical profile closely correlates to the severity of thyroid hormone deficiency and involves mostly erythropoiesis, liver function, and kidney function. Pituitary enlargement should be considered in each child with severe hypothyroidism. It is necessary to conduct prospective studies evaluating the actual frequency of anti-TSHR antibodies and pituitary enlargement in children with extremely high TSH, especially those presenting without goiters.

Aim of the study: To assess the changes in the leukocyte profile and C-reactive protein (CRP) concentration in adolescents with excess fat mass after 6-12 months of dietary intervention. Material and methods: The retrospective study included 99 overweight and obese adolescents, aged from 10.0 to 17.5 years, 82 of whom were re-hospitalized 6 to 12 months after dietary counseling. The control group consisted of 42 normal weight peers. Anthropometric measurements and laboratory tests were performed, homeostasis model assessment – insulin resistance (HOMA-IR) and triglycerides/high-density lipoprotein cholesterol (TG/HDL-C) ratio were calculated. Results: Obese and overweight adolescents had higher white blood cells (WBC), neutrophil, monocyte counts and CRP concentration. In the backward stepwise regression analysis, body mass index standard deviation score (BMI SDS) and fasting insulin concentration were independent predictors of WBC and neutrophil counts at the baseline. At the follow-up visit in 45 (54.8%) children, who had lost weight, decreases in WBC, neutrophil and monocyte counts and CRP, fasting insulin, total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG) concentrations were observed. Changes in WBC and neutrophil counts were dependent on changes in HOMA-IR and TG/HDL ratio. Changes in HOMA-IR had a significant impact on changes in the monocyte count. Conclusions: Adipose tissue promotes systemic inflammation and its intensity depends on the degree of obesity and insulin resistance. This state is reversible. Changes in HOMA-IR were independent predictors of changes in WBC, neutrophil and monocyte counts after reduction of body weight.

Serum TSH level in obese children and its correlations with atherogenic lipid indicators and carotid intima media thickness